Evidence map›Paper›PMID 25337443›Full record

ReviewInnovations in clinical neuroscience2014

Receptor Tyrosine Kinase and Tyrosine Kinase Inhibitors: New Hope for Success in Multiple Sclerosis Therapy.

Abbas Mirshafiey, Ghasem Ghalamfarsa, Babak Asghari, Gholamreza Azizi

Abstract readReview
In one paragraph

Review in Innovations in clinical neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.9field-weighted citation impact, top 29% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 30 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Abbas MirshafieyDr. Mirshafiey is from the Departmant of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran; Dr. Ghalamfarsa is from Cellular & Molecular Research Center, Yasuj University of Medical Sciences, Yasuj, Iran; Dr. Asghari is from Antimicrobial Resistance Research Center, Faculty of Medicine, Iran University of Medical Science, Tehran, Iran; Dr. Azizi is from Imam Hassan Mojtaba Hospital, Alborz University of Medical Sciences, Karaj, Iran.
Ghasem GhalamfarsaDr. Mirshafiey is from the Departmant of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran; Dr. Ghalamfarsa is from Cellular & Molecular Research Center, Yasuj University of Medical Sciences, Yasuj, Iran; Dr. Asghari is from Antimicrobial Resistance Research Center, Faculty of Medicine, Iran University of Medical Science, Tehran, Iran; Dr. Azizi is from Imam Hassan Mojtaba Hospital, Alborz University of Medical Sciences, Karaj, Iran.
Babak AsghariDr. Mirshafiey is from the Departmant of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran; Dr. Ghalamfarsa is from Cellular & Molecular Research Center, Yasuj University of Medical Sciences, Yasuj, Iran; Dr. Asghari is from Antimicrobial Resistance Research Center, Faculty of Medicine, Iran University of Medical Science, Tehran, Iran; Dr. Azizi is from Imam Hassan Mojtaba Hospital, Alborz University of Medical Sciences, Karaj, Iran.
Gholamreza AziziDr. Mirshafiey is from the Departmant of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran; Dr. Ghalamfarsa is from Cellular & Molecular Research Center, Yasuj University of Medical Sciences, Yasuj, Iran; Dr. Asghari is from Antimicrobial Resistance Research Center, Faculty of Medicine, Iran University of Medical Science, Tehran, Iran; Dr. Azizi is from Imam Hassan Mojtaba Hospital, Alborz University of Medical Sciences, Karaj, Iran.
Iran University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Receptor tyrosine kinases (RTKs) are essential components of signal transduction pathways that mediate cell-to-cell communication and their function as relay points for signaling pathways. They have a key role in numerous processes that control cellular proliferation and differentiation, regulate cell growth and cellular metabolism, and promote cell survival and apoptosis. Recently, the role of RTKs including TCR, FLT-3, c-Kit, c-Fms, PDGFR, ephrin, neurotrophin receptor, and TAM receptor in autoimmune disorder, especially rheumatoid arthritis and multiple sclerosis has been suggested. In multiple sclerosis pathogenesis, RTKs and their tyrosine kinase enzymes are selective important targets for tyrosine kinase inhibitor (TKI) agents. TKIs, compete with the ATP binding site of the catalytic domain of several tyrosine kinases, and act as small molecules that have a favorable safety profile in disease treatment. Up to now, the efficacy of TKIs in numerous animal models of MS has been demonstrated, but application of these drugs in human diseases should be tested in future clinical trials.

Indexed as

multiple sclerosisReceptor tyrosine kinasetyrosine kinase inhibitor

Identifiers

PMID25337443
PMCPMC4204472
OpenAlexW197381222

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.